Download Episcleral venous pressure in normotensive and

Volume 23
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cyclic AMP-mediated wound closure of rabbit corneal epithelium. Curr Eye Res 1:189, 1981.
8. Moses RA, Parkinson G, and Schuchardt R; A standard large wound of the corneal epithelium in the
rabbit. INVEST OPHTHALMOL VIS SCI 18:103, 1979.
9. Putt FA: Manual of Histopathological Technique.
New York, 1972, John Wiley & Sons, Inc.
10. Mishima S and Hedbys BO: Measurement of corneal thickness with the Haag-Streit pachometer.
Arch Ophthalmol 80:710, 1968.
Episcleral venous pressure in normotensive and glaucomatous beagles. KIRK N.
Fig. 1A. Isometric force-displacement transducer
with applanating Incite cone and 20 diopter lens
for the measurement of episcleral venous pressure.
GELATT, GLENWOOD G. GUM, REUBEN E.
MERIDETH, AND NANCY BROMBERC.
Episcleral venous pressure was measured by a noninvasive method with a modified force-displacement transducer in six laboratory-quality normotensive and 12
glaucomatous beagles. The dogs were anesthetized by
ketamine-xylazine, acepromazine-ketamine, and halothane. Simultaneous intraocular pressure (10?) and
blood pressure were recorded. The mean episcleral venous pressures in normotensive beagles were 11.4 to 11.6
mm Hg with the three methods of anesthesia; in the glaucomatous beagles the mean episcleral pressures were 10.6
to 12.5 mm Hg. There were no significant differences in
episcleral venous pressure (p < 0.19 and greater) and
blood pressure (p < 0.53 and greater) between the normotensive and glaucomatous beagles. IOP was significantly different between the normotensive and glaucomatous beagles anesthetized with acepromazine-ketamine
< 0.02)
(meanIOP,23.4and34.2mmHg,respectively;p
and halothane (mean IOP, 19.9 and 27.4 mm Hg, respectively; p < 0.001) but not significant with anesthesia with
ketamine-xylazine (mean IOP, 26.0 and 37.8 mm Hg,
respectively; p < 0.12). Episcleral venous pressure is unchanged as the disease progresses in the glaucomatous
beagle. (INVEST OPHTHALMOL VIS SCI 23:131-135, 1982.)
Noninvasive measurements of episcleral venous
pressure in man and animals have used direct
pressure to temporarily blanch and collapse the
vessel by various devices and a stream of air.1"4
These methods have employed a torsion balance,
pressure chamber with transparent membranes,
and force-displacement transducer. Measurement
of episcleral venous pressures in rabbits and cats
by direct cannulation under general anesthesia
yielded highly reproducible results and had a distinct end point but was an invasive procedure.5"8
Pressure-chamber methods using various membranes provided values similar to direct1 cannulation.3 The torsion-balance system, evaluated in'
Fig. IB. Position of the episcleral venous pressure
measuring system on the dog's eye.
man and rabbits, resulted in greater difficulty in
obtaining an end point and provided higher values.5 With an isometric force-displacement system, episcleral venous pressures of normotensive
and glaucomatous humans were not significantly
different.2 However, in one family with glaucoma,
episcleral venous pressure was elevated.9 The
episcleral venous pressure in persons with ocular
hypertension was significantly lower than that in
subjects with normal levels of intraocular pressure
(IOP) and glaucoma.4
Normal episcleral venous pressures in rabbits,
cats, and man range from 5 to 15 mm Hg. Pressure
chamber measurements of the episcleral venous
pressure in the dog yielded a range of 10 to 18 mm
Hg.8 The values in these species are remarkably
similar in spite of the different venous pathways of
the anterior segment.
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Invest. Ophthalmol. Vis. Sci.
July 1982
132 Reports
Table I. Mean blood pressure, IOP, and episcleral venous pressure in
laboratory-quality normotensive beagles
Blood pressure
Anesthesia
Ketamine HCl (20 mg/kg) and xylazine HCl (2 mg/kg) IV
Acepromazine maleate (0.5 mg/kg IV) and ketamine HCl (10 mg/kg IM)
Halothane
Episcleral
Systolic
Diastolic
IOP
pressure
205.0*
(10.6)
126.3
(7.3)
132.3
(5.9)
177.7
(8.0)
104.3
(5.7)
93.9
(3.6)
26.0
(2.1)
23.4
(1.5)
19.9
(0.6)
11.4
(0.7)
11.7
(0.3)
11.6
(0.4)
IV = intravenous; IM = intramuscular.
•Data expressed as mean mm Hg, with S.E.M. in parentheses.
Table II. Mean blood pressure, IOP, and episcleral venous pressure in glaucomatous beagles
Blood pressure
Anesthesia
Ketamine HCl (20 mg/kg) and xyalzine HCl (2 mg/kg) IV
Aceproinazine maleate (0.5 mg/kg IV) and ketamine HCl (10 mg/kg IM)
Halothane
Episcleral
Systolic
Diastolic
IOP
pressure
211.8*
(8.2)
122.3
(6.1)
130.3
(3.8)
183.8
(8.0)
82.2
(7.2)
96.9
(3.4)
37.8
(4.2)
34.2
(3.7)
27.4
(0.4)
12.5
(0.5)
10.6
(0.3)
12.1
(0.4)
IV = intravenous; IM = intramuscular.
*Data expressed as mean mm Hg, with S.E.M. in parentheses.
Episcleral venous pressure is an important factor in aqueous humor dynamics. This can be expressed in a rearrangement of the familiar Goldmann's classic model of aqueous humor outflow:
Po = F/C + PEVP- According to this formula, a
rise in episcleral venous pressure (PEVP), unless
compensated by a fall in the rate of aqueous humor
flow (F) or an increase in outflow facility (C), will
produce an equal rise in IOP.
In the development of the spontaneous glaucoma model in the beagle, measurement of episcleral venous pressure is imperative prior to and
during the different stages of the disease. This
study reports episcleral venous pressure, as measured by a modified force-disx^lacement transducer, in normotensive laboratory-quality beagles
and glaucomatous beagles at different stages of the
disease.
Materials and methods. Six normotensive and
12 glaucomatous beagles were evaluated by each
of three methods of anesthesia. The glaucomatous
beagles ranged in age from 13 to 100 months. A
transparent cone-shaped lucite applanation head
with a 3 mm diameter flat tip was attached to
a nearly isometric force-displacement transducer
with a maximum working range of 2 gin and a
displacement of 2.5 mm/kg (Model 03; Grass Instruments, Quincy, Mass.). The transducer with
applanating cone was mounted on a camera stand
with a joystick; magnification was provided by a 20
diopter planoconvex lens positioned 8.0 cm from
the applanating tip (Fig. 1A). The system was calibrated for each dog to provide 1 gm of force to
produce a 5 cm deflection on the recorder that was
equal to 12.5 mm Hg. Changes were displayed on
a recorder (Model 7D; Grass Instruments) with a
paper speed of 2.5 mm/sec. IOP was measured by
Mackay-Marg tonometry (Model 12; Biotronics,
Redding, Calif.) and blood pressure was recorded
by the doppler ultrasonic pressure transducer (Arteriosonde 1010; Roche Medical Electronics, Cranbury, N. J.) or by recording directly from the femoral artery.
The dogs were maintained in position by three
methods: (1) combination of 20 mg/kg ketamine HCl (Ketaset; Bristol Laboratories, Syracuse,
N. Y.), 2 mg/kg xylazine HCl (Rompun; HaverLockhart Laboratories, Shawnee, Kan.), and 0.5
mg of atropine SO4 injected slowly intravenously;
(2) 0.5 mg/kg acepromazine maleate (Ayerst Lab-
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Volume 23
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Reports 133
A
1
1
1
1
•
—
1-
—AH-
M T U O C U . M POESSUBE. " • H|
A
*•*•
H
1
h-
KTRAOCULAR PRESSURE. * • Hg
1
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Fig. 2. Distribution of the mean episcleral venous pressure and IOP of each eye of normotensive and glaucomatous beagles anesthetized with ketamine-xylazine (A), acepromazineketamine (B), and halothane (C). A, Normotensive beagles; •, glaucomatous beagles.
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134
Invest. Ophthalmol. Vis. Sci.
July 1982
Reports
oratories, New York, N. Y.) intravenously followed
5 min later by 10 mg/kg ketamine HC1 intramuscularly; or (3) general anesthesia induced with intravenous thiamylal sodium (Surital; Parke-Davis,
Detroit, Mich.) and endotracheal intubation and
maintained at a heart rate of 120 beats/min with a
mixture of oxygen and halothane (Halocarbon Laboratories, Hackensack, N. J.). The dog was positioned in lateral or dorsolateral recumbency; the
eyelids were retracted by wire eyelid speculum.
Two to three episcleral veins were selected in the
dorsal-to-dorsolateral episclera and their pressures
were measured with two to three consecutive readings (Fig. IB). The applanating cone was applied
perpendicularly to each vessel to produce blanching, but not complete collapse of the vein, while
simultaneously displaying the event on the recorder. Applanation tonometry was performed immediately before administration of the parenteral
drugs as well as before and after episcleral venous
pressure measurements.
The six normal beagles were 10 months old (two
males, two females) and 59 months old (one male,
one female). The 12 beagles with glaucoma were
13 months old (one female), 19 to 24 months old
(two males, two females), 25 to 30 months old (one
male, one female), 43 to 48 months old (two males,
two females), and 55 months old (one male). The
glaucoma was divided on the basis of clinical signs
into early, moderate, and advanced.10 Early glaucoma was present in four dogs (ages 13, 19, 20, and
22 months old), moderate glaucoma occurred in
four dogs (ages 24, 28, 29, and 43 months), and
advanced glaucoma occurred in four dogs (ages 44,
45, 48, and 55 months).
The average pressures for each episcleral vein,
IOP, and blood pressure were calculated for each
eye. The normotensive and glaucomatous beagles'
episcleral venous pressures, IOPs, and blood pressures were compared by the Student's t test. Regression analysis and Pearson correlation coefficients were used to determine the relationship
between IOP and episcleral venous pressure.
Results. The mean systolic and diastolic blood
pressure, IOP, and episcleral venous pressure of
the normotensive animals are summarized in Table I. The ranges in episcleral venous pressure
were 9.0 to 15.0 mm Hg (ketamine-xylazine), 10.0
to 12.5 mm Hg (acepromazine-ketamine), and 8.0
to 15.5 mm Hg (halothane). Under halothane anesthesia the mean difference in pressure between
two episcleral veins in the same normotensive eye
was 0.02 mm Hg. The mean difference between
pressures of episcleral veins of fellow normotensive eyes was 0.40 mm Hg (ketamine-xylazine),
1.0 mm Hg (acepromazine-ketamine), and 0.82
mm Hg (halothane).
The mean systolic and diastolic blood pressure,
IOP, and episcleral venous pressure of the glaucomatous beagles are summarized in Table II. The
ranges in episcleral venous pressure were 9.0 to
16.0 mm Hg (ketamine-xylazine), 7.5 to 12.5 mm
Hg (acepromazine-ketamine), and 9.5 to 17.5 mm
Hg (halothane). Under halothane anesthesia the
mean difference in pressure between two episcleral veins in the same glaucomatous eye was
0.03 mm Hg. The mean difference between pressures of the episcleral veins of fellow glaucomatous
eyes was 1.3 mm Hg (ketamine-xylazine), 0.6 mm
Hg (acepromazine-ketamine), and 0.3 mm Hg
(halothane).
The episcleral venous pressures of the normotensive and glaucomatous beagles were not
significantly different with any of the three methods of anesthesia (ketamine-xylazine, p < 0.61;
acepromazine-ketamine, p < 0.19; halothane, p <
0.46). IOPs of the normotensive and glaucomatous beagles were significantly different with two
anesthetic methods (acepromazine-ketamine, p <
0.02; halothane, p < 0.001) but not with the
ketamine-xylazine combination (p < 0.12). Hence
the IOPs of both the normotensive and glaucomatous groups of dogs were influenced by the choice
of anesthetic agents. The systolic and diastolic
blood pressures of the normotensive and glaucomatous beagles were not significantly different
with the three methods of anesthesia (ketaminexylazine, p < 0.59; acepromazine-ketamine, p <
0.53; halothane, p < 0.930). The systolic and diastolic blood pressures, like IOP, were directly influenced by the anesthetic method.
The distributions of IOP and episcleral venous
pressure for the normotensive and glaucomatous
beagles are summarized in Fig. 2. There were no
significant linear correlations between the right
and left eyes, the levels of episcleral venous pressure, and the levels of IOP in the normotensive
and glaucomatous dogs.
Discussion. This noninvasive method offers ease,
permits multiple recordings, and allows comparison of the results of this study to other reports.
The instrumentation is readily available, and the
special lucite applanating cone can be easily constructed. Estimation of venous pressure by collapse has inherent errors. The interposition of the
conjunctiva and reluctancy of the episcleral venous wall may result in slightly higher values.
Pressure to produce only blanching of the episcleral vein may minimize this rigidity factor.1
Movement of the eye negates the procedure,
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Volume 23
Number 1
Reports 135
necessitating sedation or general anesthesia in the
dog. Episcleral venous pressure in man is affected
by position; the recumbent pressure is at least 1
mm Hg higher than that in the sitting position.3
Regardless of the limitations of this method, differences between the normotensive and glaucomatous beagles, if present, should be detectable.
The episcleral venous pressures in the normotensive dogs, as estimated by this method,
were similar to those reported with the pressurechamber systems.7> 8 The range of 10 to 18 mm Hg
of the canine episcleral venous pressure is similar
to the intrascleral venous pressures measured by
direct cannulation in the anesthetized cat of 6.8
mm Hg (S.D. ± 0.60), with a mean IOP of 20 mm
Hg.6 In both the cat and dog the episcleral and
intrascleral vessels are related, in part, to the venous circle of Hovius, which may also branch with
the anterior ciliary and vortex veins. Whether
these anatomic differences in the anterior segment
venous pathways are important differences to man
in relationship to aqueous humor dynamics has not
been ascertained; however, it is reasonable to assume the pressures are important considerations.
Variations of the episcleral venous pressures
of the normotensive and glaucomatous Beagles
under halothane anesthesia between veins within
the same eye were not significant (p < 0.45 and
p < 0.50, respectively), supporting the reproducibility of this method. Nor were the changes different between episcleral veins of the fellow eyes in
the same dog with all three methods of anesthesia.
The lack of a significant difference of episcleral
venous pressure between the normal and glaucomatous beagles suggests the trabecular meshwork
and/or intrascleral plexus connective tissues are
the major site of resistance for the outflow of aqueous humor in inherited glaucoma in the beagle.
From the Division of Comparative Ophthalmology,
Department of Special Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville,
Fla. Supported in part by the National Institutes of
Health research grant EY01932 (Dr. Gelatt) and training
grant T32EY07060 (Drs. Merideth and Bromberg). Submitted for publication Aug. 17, 1981. Reprint requests:
Kirk N. Gelatt, Department of Special Clinical Sciences,
College of Veterinary Medicine, University of Florida,
Box J-115JHMHC, Gainesville, Fla. 32610.
Key words: Episcleral venous pressure, ocular normotensive, glaucoma, dogs
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Monocular deprivation in humans: a study of
identical twins. CHRIS A. JOHNSON, ROBERT B. POST, LEO M. CHALUPA, AND TIMOTHY
J.
LEE.
Ultrasonic axial length measurements and psychophysical
vernier acuity thresholds were determined for a pair of
identical human twins, one of whom had been monocularly deprived since birth with a congenital lens opacity.
Axial lengths of both eyes in the normal twin and the
nondeprived eye in the other twin differed by less than
0.2 mm, whereas the axial measurement of the deprived
eye was approximately 2.0 mm longer. Monocular vernier acuity thresholds in the nondeprived eye of the one
twin were not significantly different from those obtained
in the normal twin. Our findings are consistent with
previous reports of increased axial length after monocular deprivation but do not support the concept of enhanced vernier acuity in the nondeprived eye ofmonocularly deprived humans. (INVEST OPHTHALMOL VIS SCI
23:135-138, 1982.)
Since the introduction of the monocular deprivation paradigm almost two decades ago by Wiesel
and Hubel,1 a voluminous literature has documented the behavioral, anatomic, and physiologic
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